Rhinosporidiosis

This slide presentation describes the unique disease entity rhinosporidiosis

1. Rhinosporidiosis
By
Dr. T. Balasubramanian M.S.
D.L.O.

2. Definition
Rhinosporidiosis has been defined as a chronic
granulomatous disease characterized by
production of polyps and other manifestations of
hyperplasia of nasal mucosa. The etiological agent
is Rhinosporidium seeberi.

3. Rhinosporidium seeberi
•Initially believed to be sporozoan
•Classified under fungus - Olipidiaceae by
Ashworth
•Recently placed under DRIPS of aquatic
protistan parasites
•PCR tests have not demonstrated fungal
proteins

4. History
•.
1892 - Malbran observed the organism in nasal polyp
1900 - Seeber described the organism
1903 - O'Kineley described its histology
1905 - Minchin & Fantham studied O'Kineley's tissue and named
the organism as Rhinosporidium Kinealyi
1913 - ZSchokke reported similar organism in horses and named
it Rhinosporidium equi
1923 - Ashworth described its life cycle
1924 - Forsyth described skin lesion
1924 - Thirumoorthy reported the first female patient
1936 - Cefferi establised the identity of R. Seeberi and R. Equi
1953 - Demellow described the mode of its transmission

5. Incidence / geographical
description
.
More than 90% of cases have been reported
from India / Srilanka
Madurai, Ramnad, Rajapalayam, and
Sivaganga are endemic zones in Tamilnadu
Transmission is possibly due to taking bath
in common ponds

6. Theories of spread
.
•Demellow's theory of direct transmission
•Autoinoculation theory of Karunarathnae
(responsible for satellite lesions)
•Haematogenous spread - to distant sites
•Lymphatic spread - causing lymphadenitis
(rarity)

7. Karunarathnae ‘s theory
.
Karunarathnae postulated that Rhinosporidium
seeberi existed in a dimorphic state. It existed in
a saprophytic form in soil and water. It took a
yeast form inside tissues. This ability to exist in
dimorphic state helps it to survive hostile
environment for a long period of time.

8. Reasons for endemicity
.
•Physical characteristics of water in the
ponds
•Presence of synergistic aquatic
organisms
•Genetic predisposition in patients
affected
•Host immunity (lack of) or altered

9. Life cycle (Ashworth)
.
•Spore is the basic infecting unit.
•It is about 7 microns in size
•Also known as spherule
•It has clear cytoplasm with 15 – 20 vacuoles filled
with food matter
•It is enclosed in a chitinous membrane
•Found only in connective tissue spaces and is
rarely intracellular

10. Life cycle (Ashworth)
.
•Spores start to increase in size
•At 50 – 60 microns size granules start to appear.
Nucleus prepares for cell division
•Mitosis occur 4, 8, 16, 32 and 64 nuclei are
formed
•At 7th division size becomes 100 microns
•Fully mature sporangium is 150 microns
•Mature spores are found in the centre and
immature ones at the periphery

11. Life cycle (Ashworth)
.

12. Life cycle (Recent)
.
•Trophozoite (Juvenile sporangium) – 6 – 100 microns
•It has single nucleus at 6 µ stage / Multiple nuclei at
100 µ stage
•Lipid granules are seen in cytoplasm

13. Life cycle (Recent)
.
1. Intermediate sporangium is 100 – 150 µ in diameter
2. It has bilamellar cell wall – outer chitinous and inner
cellulose
3. Immature spores are seen within the cytoplasm
4.There are no mature spores seem inside the cytoplasm

14. Life cycle (Recent)
.Mature sporangium:
•100 – 400 microns
•Cell wall is thin and bilamellar
•Inside cytoplasm mature and immature spores are seen
•These spores are embedded in mucoid matrix
•Bilamellar cell wall has one weak spot – operculum
•Spores mature in centrifugal and centripetal pattern
•Mature spores are covered with mucoid material (comet
of Beattee)
•Mature spores give rise to electron dense granules
which are the ultimate infecting unit

15. Life cycle (Recent)
.

16. Clinical classification
.
• Nasal
• Nasopharyngeal
• Mixed
• Bizzarre (ocular and genital)
• Malignant rhinosporidiosis (cutaneous rhinosporidiosis)

17. Common sites affected
.
Nose - 78%
Nasopharynx - 68%
Tonsil - 3%
Eye - 1%
Skin - very rare

18. Features of nasal Rhinosporidiosis
•Lesions are polypoidal reddish and
granular
•Lesions may be multiple, pedunculated
and friable
•Surface is studded with whitish dots i.e.
sporangia
•The nasal lesions are highly vascular and
bleeds on touch
•The whole mass could be seen to be
covered with mucous secretion
•The lesion is restricted to nasal mucous
membrane and does not cross the
mucocutaneous junction

19. Histopathology of nasal
Rhinosporidiosis
•Papillomatous hyperplasia of mucous
membrane with rougae formation
•Epithelium over sporangia is thinned out
and giant cells could be seen in this area
•Accumulation of mucous in the crypts
•Increased vascularity due to
angiogenesis factor
•These spores stain with sudan black,
Bromphenol blue

20. Features of nasal Rhinosporidiosis
•Chronicity
•Recurrence
•Dissemination

21. Reasons of chronicity
•Antigen sequestration
•Antigenic variation
•Immune suppression
•Immune distraction
•Immune deviation
•Binding of host
immunoglobulins

22. Treatment
•Surgery
•Dapsone 100 mg /day –
6 months

23. .